《口腔颌面外科杂志》

• 基础研究 • 上一篇    下一篇

miR-30e-5p调控口腔鳞癌细胞增殖和迁移的实验研究

朱雪琴, 叶冬霞, 秦 星, 陈万涛   

  1. 国家口腔疾病临床研究中心,上海市口腔医学重点实验室,上海市口腔医学研究所,上海交通大学医学院附属第九人民医院口腔颌面头颈肿瘤科,上海 200011
  • 出版日期:2018-06-28 发布日期:2019-11-28
  • 通讯作者: 陈万涛,教授. E-mail: chenwantao196323@sjtu.edu.cn
  • 作者简介:朱雪琴(1990—),女,湖北黄石人,硕士. E-mail: 964674542@qq.com
  • 基金资助:
    国家重点研发计划(2016YFC0902700);国家自然科学基金项目(81472515)

miR-30e-5p Regulates Proliferation and Migration of Oral Squamous Cell Carcinoma

ZHU Xue-qin, YE Dong-xia, QIN Xing, CHEN Wan-tao   

  1. Department of Oral and Maxillofacial-Head and Neck Oncology and Faculty of Oral and Maxillofacial Surgery, Ninth People’s Hospital, College of Stomatology, Shanghai Jiaotong University School of Medicine, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of Stomatology, Shanghai 200011, China
  • Online:2018-06-28 Published:2019-11-28

摘要: 目的:研究miR-30e-5p对口腔鳞癌细胞增殖和迁移能力的影响,探讨其在口腔鳞癌发生发展中的作用。方法:实时荧光定量PCR检测miR-30e-5p在人口腔鳞癌组织、癌旁组织、正常口腔黏膜上皮细胞和HN6细胞系中的表达水平。应用miR-30e-5p mimics、miR-30e-5p inhibitor、mimics NC、inhibitor NC分别转染HN6细胞,实时荧光定量PCR检测转染后miR-30e-5p的表达变化;采用细胞增殖实验、平板克隆形成实验、划痕实验分别检测miR-30e-5p对HN6细胞生长和迁移的影响。结果:相对于癌旁正常组织,miR-30e-5p在口腔鳞癌组织中的表达显著下调(P<0.05)。相对于正常口腔黏膜上皮细胞,miR-30e-5p在口腔鳞癌组织中的表达显著下调(P<0.05)。转染miR-30e-5p mimics后,HN6细胞的增殖能力、克隆形成能力及迁移能力显著降低,而转染miR-30e-5p inhibitor后,HN6细胞的增殖能力、克隆形成能力及迁移能力则明显升高,差异均具有统计学意义(P<0.05)。结论:miR-30e-5p在口腔鳞癌组织中低表达,与口腔鳞癌细胞的生长和迁移密切相关,提示miR-30e-5p在口腔鳞癌的发生、发展过程中可能起抑癌基因的作用。

关键词: miR-30e-5p, 口腔鳞癌, 增殖, 迁移

Abstract: Objective: The aim of this study was to investigate the effects of miR-30e-5p on the proliferation and migration of tumor cells in oral squamous cell carcinoma (OSCC), and to determine its role in OSCC progression. Methods: The expressions of miR-30e-5p in OSCC tissues, adjacent normal tissues, normal oral mucosal epithelial cells and HN6 cells were individually examined by real-time quantitative PCR. The miR-30e-5p mimics, miR-30e-5p inhibitor, mimics NC and inhibitor NC were transfected into HN6 cells, respectively. Transfection efficiency and expression level of miR-30e-5p were detected by quantitative real-time PCR assay. The proliferation assay, plate colony formation assay and wound healing assay were performed to study the effects of miR-30e-5p on cell proliferation and migration. Results: The expressions of miR-30e-5p was down-regulated in OSCC tissues when compared with the paired normal tissues (P<0.05). Similarly, the expressions of miR-30e-5p was down-regulated in HN6 cells when compared with the normal oral mucosal epithelial cells (P<0.05). Overexpression of miR-30e-5p in HN6 cells significantly inhibited the proliferation, colony formation and migration abilities of HN6 cells (P<0.05); while silencing of miR-30e-5p by miR-30e-5p inhibitor in HN6 cells remarkably promote the proliferation, colony formation and migration abilities of HN6 cells (P<0.05). Conclusions: miR-30e-5p was down-regulated in OSCC and the expression of miR-30e-5p was correlated with the proliferation and migration of tumor cells, which indicated that miR-30e-5p may play a vital role as tumor suppressor gene during the development and progression of OSCC.

Key words: miR-30e-5p, oral squamous cell carcinoma, proliferation, migration

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